Matías Fuentealba

The paper shows that simulated microgravity causes aging-like transcriptional changes in human organoids, with effects varying by tissue type.

The paper develops methods to infer organ aging, senescence, and hallmark scores from blood transcriptomes and facial photographs, showing associations with mortality.

This study shows that oral DBM treatment prevents cognitive decline in a C9ORF72 FTD mouse model without altering protein inclusions but corrects gene expression changes related to cytoskeleton, ALS, and metabolism.

This study uses UK Biobank data to develop an 18-year mortality risk estimator for domain-specific intrinsic capacity, identifying immune system activation across domains.

This study uses simulated microgravity to model biological aging in humans, finding similar transcriptional changes to natural aging across multiple systems and aging hallmarks.

The paper identifies a distinct p16INK4a-associated senescence signature in human ovarian tissue through proteogenomic profiling and spatial analysis.

The paper develops a DNA methylation-based epigenetic clock to predict mortality and associate with clinical, immunological, and lifestyle factors related to intrinsic capacity.

The paper develops mortality-based predictors of biological age for 9 physiological systems using blood data from the UK Biobank and validates them in the Health and Retirement Study.

This study shows that expressing human amyloid-β and Tau in C. elegans neurons causes phenotypic and multi-omic changes, including accelerated aging and metabolic dysfunction.

The paper shows that manipulating the UPR pathway can restore brain function and reduce aging-related deficits.

This study identifies genetic associations between age-related diseases, finding four clusters with shared age-of-onset profiles and aging-related genes, and suggests drug repurposing for multiple age-dependent diseases.

This study compares transcriptomic changes in long- and short-lived mouse models of ageing, identifying mitochondrial metabolism as a key factor and showing that progeroid mice exhibit gene expression patterns similar to normal ageing.

The paper identifies anti-ageing drug candidates by analyzing drug-protein interactions and validates one candidate in C. elegans.

This study uses gene expression data to identify drugs that may combat ageing by comparing age-related gene changes with drug-induced profiles.